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A 57-year-old man with herpes zoster oticus developed a delayed fourth nerve palsy followed by transient intermittent sixth nerve weakness. Trochlear nerve lesions occur rarely with zoster, particularly in the absence of zoster ophthalmicus. A knowledge of the wide range of motor manifestations and the chronicity of meningitis with zoster will afford earlier diagnosis without resort to arteriography.
Cryptic angiomas, which are intrinsic to cranial nerves, are uncommon. Such lesions involving the trochlear nerve have not been previously described. The authors have therefore found it interesting to report a case fortuitously discovered in a patient with trigeminal neuralgia who underwent a fifth nerve microvascular decompression through the supracerebellar space. The angioma was not responsible for the neuralgia, but because of its potential risk of bleeding, the lesion was treated by resection of the trochlear nerve in its invaded portion. Then, the nerve was successfully repaired with an autograft harvested from the distal part of the sural nerve.
We report a case of trochlear nerve palsy that was the sole initial sign of an aneurysm of the superior cerebellar artery. A craniotomy confirmed the anatomical compression of the trochlear nerve by this aneurysm. The clipping of the aneurysm resulted in the resolution of the trochlear nerve palsy.
The clinical course of six patients with isolated trochlear nerve palsy as the only ocular motor manifestation of herpes zoster ophthalmicus has been analyzed. Spontaneous recovery occurred in only three. Review of the literature does not clarify the mechanism of such palsies, which potentially may result from the following conditions: local orbital muscle inflammation and ischemia; contiguous intracavernous spread of inflammation from the trigeminal nerve; and a concurrent but independent motor neuropathy or ganglionitis.
Complete return of function has been obtained following neurosurgical repair of a trochlear nerve inadvertently divided during the clipping of a basilar tip aneurysm. To date this is the second case reported in the literature. The technique of repair and the method of recording the return of function is discussed.
Development of the trochlear nerve from day 11 of incubation through hatching was studied in white Peking duck embryos. Counts of fibers from the electron micrograph montages indicate that initially there is an abundant collateral sprouting which roughly coincides with the time of neuromuscular contacts, suggesting some sort of interaction between the developing nerve and the periphery. The maximum number of trochlear cells and fibers is present on day 12. Average cell and fiber counts on this day are 2325 and 47,386 respectively. Assuming all cells send their axons into the nerve and that all cell bodies are present within the trochlear nucleus, the ration of cells to fibers is 1:20. Average cell and fiber counts at hatching are 1338 and 1506 respectively. Thus, losses of approximately half the trochlear cells and of 97% of the fibers occur during normal development. Degenerating cells and fibers are first observed on day 13. Degeneration involves both the myelinated and the unmyelinated axons. The actual number of degenerating fibers which were observed, however, was very small compared to the number of fibers lost during development; thus, it is suggested that, in the majority of cases, fiber loss is perhaps via retraction of axon collaterals. In general, cell death slightly precedes axon loss, which suggests that the direction of the degeneration is from cell body to the axon. A cell/fiber ratio of approximately 1:1 is first observed on day 18 and remains so thereafter. Indirect evidence is discussed, suggesting that at least some cells which die during normal devleopment had sent their axon into the nerve prior to their death. Whether these axons make meaningful connections with the muscle is uncertain.
Complete axonal counts have been made in the intracranial parts of trochlear nerves from human fetuses of 9.2, 10 and 24 cm crown-rump length. A count was also made in the intraorbital part of the nerve from the 10 cm specimen. Schwann cell nuclei were also counted in typical cross sections, but do not necessarily reflect very accurately the schwann cell contents of the nerves. Axonal numbers conform to the propositions (1) that they do not all grow out at once, (2) do not all survive and (3) that degeneration may occur before or after myelination has begun. It seems inevitable that some loss of Schwann cells occurs in relation to the degeneration of myelinated axons, but there is no evidence for or against such a loss in relation to the degeneration of unmyelinated axons. Overall, however, Schwann cell numbers tend to increase as the number of myelinated axons increases.
A case of trochlear nerve palsy in herpes zoster ophthalmicus is presented. The rarity of fourth nerve involvement in herpes zoster is emphasized.
As a part of a continuing study of the relationship between age and neuronal population within the human brain stem, the nucleus of the trochlear nerve was examined in a total of 20 brains from newborn to 87 years of age. The cell count in the newborn was 1,830, and in the 87-year-old 2,010, while the mean number for all the specimens examined was 2,115. It is apparent that there is no cell loss in this nucleus in the normal aging process, which is in accord with the findings in five other brain stem nuclei examined by various investigators. This is in contrast to the findings in cerebral and cerebellar cortex which show significant cell loss with advancing age. Based on this and previous studies of the brain stem nuclei, it appears that neuronal loss is not a concomitant of the normal aging process in the brain stem. The anatomical basis of this selectivity in neuronal loss with aging in certain parts of the brain is not known at present.
Trochlear nerves from two human fetuses, and digital nerves from a third, have been examined by electron microscopy. Very marked differences in maturation were found between trochlear nerves of fetuses of ages differing only by 2--3 weeks, and between proximal and distal parts of the same trochlear nerve. Immaturity was reflected in paucity of endoneurial space and collagen and in the rarity, or virtual absence, of endoneurial fibroblasts. Circumstantial evidence of collagen formation by Schwann cells has been presented and discussed.
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Superior oblique muscle/trochlear nerve pairs from goldfish of various ages (1-5 years) have been examined light and electron microscopically. The muscle grows by enlargement (longitudinally and transversely) of individual fibers, and by addition of new ones at the rate of about 250/year. The nerve grows by enlargement of fibers, but few and perhaps no new axons are added. The somata enlarge, and the neuromuscular synapses become much more numerous. The ratio of muscle fibers to nerve fibers increases from about 5 in the young to about 16 in the old fish.
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At the McGill University neuro-ophthalmology unit, 52 patients with superior oblique palsy were seen during the 2-year period October 1973 to August 1975; these included patients with congenital, traumatic, vascular, and other more rare causes of trochlear paralysis. Half of the patients with congenital palsy had diplopia, requiring treatment, although surgery was rarely necessary. Patients with palsy due to trauma, the major cause in our series, included four with bilateral involvement. With the exception of recovery in a single muscle of one patient in this group with traumatic palsy, no spontaneous recoveries have been observed. Treatment modalities have been tried, including observation alone, occlusion for symptomatic relief of diplopia, use of prisms, and recession of the ipsilateral inferior oblique muscle. Four patients with palsy of presumed vascular cause recovered spontaneously within a 4-month period. All patients who were surgically treated improved.